17beta-estradiol, but not raloxifene, decreases thrombomodulin in the antithrombotic protein C pathway.
Endocrinology
; 141(10): 3908-11, 2000 Oct.
Article
em En
| MEDLINE
| ID: mdl-11014248
ABSTRACT
Raloxifene is a nonsteroidal selective estrogen receptor modulator (SERM) that mimics the effects of estrogen on some plasma lipids and may have direct effects on the vascular wall. The objective of this study was to determine the effects of 17beta-estradiol, raloxifene, and LY139,478 (a related benzothiophene SERM) on the anticoagulant protein C pathway. In human vascular endothelial cells activated with interleukin-1 (IL-1), we demonstrated decreased thrombomodulin-dependent protein C activation. 17beta-estradiol reduced the anticoagulant properties of both unstimulated and IL-1-activated endothelial cells by decreasing thrombomodulin expression. In contrast, raloxifene and LY139,478 enhanced the anticoagulant properties of both unstimulated and IL-1-activated endothelial cells through upregulation of thrombomodulin. Regulation of the protein C pathway via thrombomodulin on vascular endothelium may be a novel mechanism by which SERMs could potentially confer cardioprotective effects and reduce the thrombotic risk associated with HRT in compromised patients.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Trombose
/
Proteína C
/
Trombomodulina
/
Cloridrato de Raloxifeno
/
Estradiol
/
Antagonistas de Estrogênios
Limite:
Humans
Idioma:
En
Revista:
Endocrinology
Ano de publicação:
2000
Tipo de documento:
Article